Akt/FoxO通路介导的线粒体损伤在脑卒中后肌少症中作用的研究进展  

Research Progress of Mechanism of Akt/FoxO Pathway Mediated Mitochondrial Damage in Post-Stroke Sarcopenia

作　　者：任欢欢 杨雪 姚黎清[1] REN Huanhuan;YANG Xue;YAO Liqing(Department of Rehabilitation Medicine,the Second Affiliated Hospital of Kunming Medical University,Kunming 650101,China)

机构地区：[1]昆明医科大学第二附属医院康复医学科,昆明650101

出　　处：《医学综述》2025年第6期647-651,657,共6页Medical Recapitulate

基　　金：国家自然科学基金(82460453);云南省贾杰专家工作站(202305AF150032)。

摘　　要：脑卒中是全世界成人残疾和死亡的主要原因,脑卒中后肌少症是脑卒中患者常见的并发症,表现为肌量减少和肌力下降,严重影响患者的康复和生活质量,但其发生机制尚未完全明确。蛋白激酶B(PKB/Akt)/叉头框转录因子O(FoxO)通路在脑卒中后肌少症中发挥关键作用。Akt/FoxO信号通路通过调控骨骼肌细胞的生长和代谢,介导肌肉萎缩;通过调控线粒体功能和质量控制,影响肌肉细胞的能量代谢,促进或抑制肌少症的发生。尽管当前研究揭示了Akt/FoxO通路在脑卒中后肌少症中的潜在作用,但其具体机制仍不完全清楚。未来的研究应聚焦于该通路的调控网络以及药物干预的潜力,通过调节Akt/FoxO通路减缓脑卒中后肌少症的发生和发展,以为临床治疗提供新的靶点和策略。Stroke is the leading cause of disability and death among adults worldwide.A common complication in stroke patients is post-stroke sarcopenia,which is characterized by a decrease in both muscle mass and muscle strength,seriously impairing the recovery and quality of life of the patients.However,the underlying mechanisms remain not fully understood.The protein kinase B(PKB/Akt)/forkhead box transcription factor O(FoxO)pathway plays a crucial role in post-stroke sarcopenia.The Akt/FoxO pathway mediates muscle atrophy by regulating the growth and metabolism of skeletal muscle cells.It also influences energy metabolism in muscle cells through the regulation of mitochondrial function and quality control,thereby promoting or inhibiting the development of sarcopenia.Although current studies have revealed the potential involvement of the Akt/FoxO pathway in post-stroke sarcopenia,its specific mechanisms is still not fully understood.Future research should focus on elucidating the regulatory network of this pathway and exploring the potential for pharmacological interventions that could slow the onset and progression of post-stroke sarcopenia by regulating Akt/FoxO pathway,so as to offer new targets and strategies for the clinical treatment.

关 键 词：脑卒中 肌少症 蛋白激酶B/叉头框转录因子O通路 线粒体损伤 

分 类 号：R743.3[医药卫生—神经病学与精神病学] R685.4[医药卫生—临床医学]